Exercise-Induced Pulmonary Hemorrhage

In exercise-induced pulmonary hemorrhage (EIPH) blood is present in the airways after exercise. The most frequent classification of horses as exercise-induced pulmonary hemorrhage positive or negative is currently based on postexercise endoscopy. Until the introduction of endoscopy and surveys of horses after racing, it generally was considered that only few horses experienced exercise-induced pulmonary hemorrhage, and the occurrence was based only on the appearance of blood at the nostrils (epistaxis). Even today, the lay perception of a horse classified as a “bleeder” is frequently that of an animal that either has profuse amounts of blood in the trachea after training or racing or exhibits epistaxis.

However, exercise-induced pulmonary hemorrhage should now be considered ubiquitous in horses undertaking fast or intense exercise. The range of the condition varies from horses showing only a small increase in the number of red blood cells detectable in the airways using sensitive techniques such as bronchoalveolar lavage (bronchoalveolar lavage) to those showing marked epistaxis, with all grades in between. Whether all gradations of exercise-induced pulmonary hemorrhage share a common etiology is unknown.

Some debate exists as to the intensity of exercise required to induce exercise-induced pulmonary hemorrhage. Hemosiderophages are present in the tracheal wash of all horses in training when galloping. More recently, studies showed that lesions consistent with exercise-induced pulmonary hemorrhage were present in the lungs post mortem of 10 of 13 Thoroughbred horses aged less than 2 years that had been trained at speeds of only 7 to 8.5 m/s (420-510 m/min or 16-19 mph). In addition, 100-fold increases occur in red blood cell numbers in bronchoalveolar lavage taken after treadmill exercise at only 600 m/min (22.5 mph), but without blood being present in the trachea.

Although for many years seen as a condition affecting the Thoroughbred racehorse, it is now clear that exercise-induced pulmonary hemorrhage occurs in any horse undertaking fast or intense exercise, including Thoroughbred racing on turf or dirt, racing over jumps (hurdle and steeplechase), 3-day eventing, polo, barrel racing, reining, roping and cutting, Quarter Horse racing, Appaloosa racing, Arab racing, Standardbred racing (pacing and trotting), show-jumping, and even in draught and endurance horses. The greater the severity of exercise-induced pulmonary hemorrhage the greater is the implication for health and welfare. In addition, moderate to severe exercise-induced pulmonary hemorrhage commonly is thought to be a contributing factor in poor performance.

However, despite considerable anecdotal evidence, only one study has found that severe endoscopic exercise-induced pulmonary hemorrhage was less common in placed than in unplaced horses. A recent report showed that the incidence of endoscopic exercise-induced pulmonary hemorrhage in a group of 166 horses examined immediately postrace in the United Kingdom (flat and jump racing) because of poor performance was no different than that of controls (horses performing to expectation). In addition, no relationship existed between exercise-induced pulmonary hemorrhage incidence or severity and finishing position in either the control (223 horses) or poor performance group.

In most cases, exercise-induced pulmonary hemorrhage affects the pulmonary circulation, although severe episodes of exercise-induced pulmonary hemorrhage may involve disruption of the bronchial circulation. In 2- to 3-year-old Thoroughbred racehorses, post mortem examination of the lungs reveals lesions consistent with exercise-induced pulmonary hemorrhage almost exclusively in the tips of the dorsocaudal lung. These may be visible on gross examination or only on histologic examination using microscopy. With increasing age, there is a pattern for the lung to be stained a dark brown-blue (because of repeated and extensive hemosiderin deposition) and for the area of lung affected to be more extensive. The areas of staining are often approximately symmetric in the left and right lung and often may extend to the most cranial regions along the medial spinal surface of both lungs.

A number of endoscopic surveys of exercise-induced pulmonary hemorrhage in racehorses have described the incidence (i.e., the chance that an individual horse on a single occasion will have blood in the trachea postexercise) as being between 30% and 80%. If multiple examinations are made on the same horse, the incidence rises to 82% to 95%. The endoscopic incidence of exercise-induced pulmonary hemorrhage has been shown to increase from 40% in 2-year-old Thoroughbreds racing on grass, to 65% in 3-year-olds and 82% in horses ages 4 and older.

The incidence of epistaxis associated with Thoroughbred and Arabian racing in Japan recently was reported to be 0.15%. Risk factors for epistaxis included jump-racing, age greater than 2 years, race distances of less than 1600 m (1 mile), and female gender. The recurrence rate in individual horses was relatively low (4.6%). In contrast to endoscopic exercise-induced pulmonary hemorrhage and performance, externally visible epistaxis was shown to have a significant effect on the performance of Thoroughbred racehorses in Korea.

Etiology of Exercise-Induced Pulmonary Hemorrhage

Effects Of Exercise-Induced Pulmonary Hemorrhage

Instillation of autologous blood into the airways causes inflammation and has been characterized by an early neutrophil influx. Although severe bleeding and visible epistaxis are probably now generally considered to affect performance, the effect of the “average” severity of bleeding is still unclear. Instillation of 200 ml of autologous blood (but not saline) into each lung decreases maximal oxygen uptake and by implication, would be expected to affect performance. However, how these acute experimental inoculations relate to natural exercise-induced pulmonary hemorrhage is unknown.

Diagnosis of Exercise-Induced Pulmonary Hemorrhage

Treatment of Exercise-Induced Pulmonary Hemorrhage